AJP - Heart and Circulatory Physiology, Vol 248, Issue 5 652-H657, Copyright © 1985 by American Physiological Society
Role of vasopressin and sympathetic nervous system during hypertonic NaCl infusion in conscious dog
E. M. Hasser, J. R. Haywood and V. S. Bishop
The contribution of arginine vasopressin (AVP) and the sympathetic nervous
system to the pressor response elicited by hypertonic NaCl infusion was
investigated in conscious dogs with intact carotid sinus baroreceptors or
in dogs subjected to chronic sinoaortic baroreceptor denervation (SAD).
Infusion of 6% NaCl at 0.05 ml X kg-1 X min-1 for 60 min increased plasma
osmolality an average of 12 +/- 2 mosmol/kg in both intact and SAD dogs.
Arterial pressure increased 6 +/- 2 mmHg in intact animals and was
normalized by subsequent administration of a specific vascular AVP
antagonist. Pretreatment with the AVP antagonist did not alter resting
arterial pressure but prevented the increase due to the osmotic stimulus.
Pretreatment with ganglionic blockade reduced resting arterial pressure
(-17 +/- 2 mmHg). Subsequent infusion of hypertonic NaCl elevated arterial
pressure (21 +/- 7 mmHg) to a significantly greater level than that
observed with the autonomic nervous system intact. In SAD dogs, the osmotic
stimulus increased arterial pressure (16 +/- 1 mmHg) to a significantly
greater extent than in intact animals. Subsequent administration of AVP
antagonist normalized arterial pressure, and pretreatment with the
antagonist prevented any pressor response. Pretreatment with ganglionic
blockade did not alter the pressor response (15 +/- 2 mmHg) to hypertonic
NaCl. Data suggest that the increase in arterial pressure due to an osmotic
stimulus is due to AVP release and does not require a functional
sympathetic nervous system. The response is normally buffered by arterial
baroreflexes, presumably due to sympathetic withdrawal.
